MOTS-C nothing more. nothing less.
MOTS-c is a mitochondrial-derived peptide encoded within the 12S rRNA region. Studied in research involving mitochondrial signaling, AMPK activation, metabolic stress response, and cellular energetics.
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About This Compound
Deep technical insights for clinical research
Primary Research Applications
This compound is supplied strictly for in-vitro and preclinical research use only. Primary applications include the areas below.
Activates AMPK pathway to enhance mitochondrial biogenesis and restore metabolic homeostasis in insulin resistance models.
Reverses age-dependent insulin resistance and obesity through preservation of metabolic flexibility and mitochondrial respiration.
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Pairs & Supplies
The compounds and tools researchers stack with MOTS-C.
Peer-Reviewed Literature
Related Studies
MOTS-c Is an Exercise-Induced Mitochondrial-Encoded Regulator of Age-Dependent Physical Decline and Muscle Homeostasis
Nature Communications
MOTS-c enhanced physical performance across the lifespan; in aged mice (equivalent to 65+ years), it doubled running capacity by regulating nuclear gene expression in skeletal muscle.
The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance
Cell Metabolism
Foundational study identifying MOTS-c as a novel mitochondrial-derived peptide that prevents age- and diet-induced insulin resistance through AMPK activation via folate cycle inhibition.
Mitochondrial-Encoded Peptide MOTS-c Prevents Pancreatic Islet Cell Senescence to Delay Diabetes
Experimental & Molecular Medicine
MOTS-c reduced senescence markers in aged pancreatic islets and improved glucose intolerance in diabetic mice. Circulating MOTS-c levels are lower in T2D patients versus healthy controls.
MOTS-c Is an Exercise-Induced Mitochondrial-Encoded Regulator of Age-Dependent Physical Decline and Muscle Homeostasis
Nature Communications
MOTS-c levels increase with exercise, and exogenous MOTS-c administration in aged mice improved physical capacity, grip strength, gait, and thermogenesis to levels approximating young controls.
MOTS-c Peptide Regulates Adipose Homeostasis to Prevent Ovariectomy-Induced Metabolic Dysfunction
Journal of Molecular Medicine
MOTS-c treatment prevented ovariectomy-induced obesity and insulin resistance by promoting brown adipose tissue activation, improving glucose tolerance, and reducing visceral fat accumulation.
The Mitochondrial-Derived Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress
Cell Metabolism
MOTS-c translocates to the nucleus under metabolic stress to directly regulate ARE-containing genes via AMPK-dependent chromatin remodeling — establishing a novel mito-nuclear communication pathway.
From the Lab
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